Day 6 Dermatology Flashcards
What is the difference between a macule and a papule?
What is a patch vs a plaque?
What is a wheal vs a nodule?
macule is small and different in color than skin, papule is raised and different in color, also small.
patch- different in color, scales and fine wrinkles(>1 cm), plaque is a big papule.
Wheal–> caused by eczema, transient and itchy. Nodule–> solid, greater than .5 cm in depth and width
What is a vesicle vs a bulla?
What is a scale?
What is a fissure vs erosion vs ulcer?
Vesicle is fluid filled .5.
loose cells, white and dry.
Fissure–> thin and may expose the dermis, erosion are wide and limited to the epidermal . Ulcers go beyond the epidermal layer to the dermal layer or beyond.
What is a petechiae vs a purpura?
What is an eccymosis?
What is an uritcaria?
Petechiae are small and purpura are large, both are non blanching.
Larger than purpura, flat, purple.
IgE mediated eruption with abrupt onset, dissaperance(within 24 hours), can be brought on by drugs.
What is phototoxicity?
What is contact dermatitis?
What is the clinical presentation of atopic dermatitis?
combination of a drug and a light source, drugs that can cause are tetracyclines, coal tar, some fluoroquinolines, sulfonamides, HCTZ, and phenothiazines.
delayed, 5-7 days to sensitize, quicker onset w/second exposure, parabens, benzocaine, neomycin, topical antihistamines, PABA.
Childhood-infants- age 5. Resolving by adulthood in all but 10-30%. 80% mild. Inflammation and itching, relapsing and remitting, food allergies, asthma, allergic rhinitis, itching, xerosis, elevated IgE, red, edematous, broken, oozing, crusting skin.
What is lichenification?
What are some secondary problems of atopic dermatitis?
What are some risk factors for atopic dermatitis?
When skin becomes leathery due to scratching in atopic dermatitis.
chronic tiredness, growth retardation, psychological problems.
Higher latitude, cold temps, dry air, black race. Exacerbated at high temps, stress, heat, sweat, wool clothing, overlapping contact dermatitis.
What’s the pathophysiology of atopic dermatitis?
What are occlusives vs humectants vs emollients?
What are your occlusive agents?
Type 2 T helper cell activation, release of IL-4,5,10,13. Prostaglandin E2 stimulates IgE from B cells, Keratinocyte disruption. further attracts T cells. Low fillagrin.
Occlusives hold moisture in(preferred), humectants increased water holding capacity(stinging, not preferred), emollients(contain droplets of oil, don’t do much).
Petrolatum, dimethicone, mineral oil.
Is water or fat based preferred?
What is wet wrap therapy?
What is AD treatment mainstay?
Water needs a preservative and can cause stinging so fat based preferred.
Soak wraps, bathe child in warm water and use a gentle cleanser, lightly pat child’s skin, apply lotion within 3 minutes, wring out excess water from wrap and immediately dress child, apply a dry layer of clothing.
Corticosteroids, high potency to quick control, taper or lowest potency with efficacy, can use for active disease or prevention of relapse.
What are AE’s of corticosteroids?
What are the calcineurin inhibitors you can use in AD?
What special things to know about calcineurin inhibitors?
Purpura, acneiform or rascea looking areas, telangiectasia, striae, skin atrophy. Treat once-twice a week to prevent relapse.
Picrolimus, tacrolimus. Efficacy comparable to corticosteroids.
Intermittent use, should only be used on affected areas.. Use steroid first in acutely inflammed skin, risk of malignacy, no blood monitoring, lower strength of tacrolimus <2 years.
What is your 3rd line therapy in AD and 4th line therapy in AD?
What is not recommended in AD?
What is the pathophysiology of psoriasis?
3rd line is UV light, 4th line is systemic immunomodulating agents.
Biologic therapy, antibacterial stuff, steroids plus a topical antibiotic, coal tar, topical antihistamines.
2% of the population reporting disease, autoimmune, gene encoding HLA-Cw6(13x higher risk), Family History.
What are psoriatic triggers?
What is the mechanism of psoriatic trigger?
What is the koebner phenomenon?
Stress, Meds(beta blockers, NSAIDS, antimalaralias, lithium, ACEI, interferons),Trauma, Infection.
LL37–> trigger pro inflammatory mediators produced by keratinocytes–>TH17 and other cells containing IL-17 cause it.
psoriasis shows up at old injury.
Do infections flare psoriasis?
What is the presentation of psoriasis?
Where does psoriasis show up?
Yes, streptococcal pharyngitis.
Red papules and plaques, itchy, distinct borders, thick scale, round or oval lesions, pinpoint bleeding when scale is removed, center of lesion clears first.
scalp,elbows,knees,hands,feet,genitalia, lower back.
What is the maximum PASI scores?
What are psoriasis’s comorbidities?
What is a mainstay treatment in psoriasis?
72, Newest medications PASI 75- or higher.
hepatoxicity,metabolic syndrome, cardiovascular disease, etc.
corticosteroids–> once daily until remission is okay, 2 weeks to benefit with high potency, tachyphylaxis or rebound disease can occur after a few weeks so more intermitten dosing is required for long therapy.
What is another 1st line treatment in psoriasis?
How does calcipotriene work in psoriasis?
How does tazarotene work in psoriasis?
Vitamin D3.
more expensive but safe long term.
topical retinoid that is 2nd line therapy.
Can calcineurin inhibitors work in psoriasis?
How does photo(chemo)therapy work in psoriasis?
What are methotrexate safety concerns?
YES, use in skin folds and on the face where steroids are avoided.
Moderate to severe. Phototherapy=UVB alone, Photochromotherapy=UVA+PSORALEN=PUVA–> Skin cancer not combined with immunosuppresives, teratogenic.
LIVER!!!!!, blood cells and platelets, pulmonary(rare), teratogenic. GIVE FOLIC ACID.
What do you watch for with sulfasalazine?
What do you watch for with cyclosporine?
What to watch for with apremilast?
Hepatotoxicity, sulfa or aspirin allergy, reduced blood cell counts.
Renal, hypertension, lipids, needs to be tapered.
Oral, diarrhea, vomiting, nausea, depression, weight loss, CYP3A4 substrate.
Can you use TNF inhibitors for psoriasis?
What other biologics can you use?
What do you see in psoriatic arthritis?
YES, Adalimumab, etanercept, infliximab.
IL-17, IL-23.
Spondylitis, Enthesitis, Dactylitis(sausage digits).
What is mild disease(<3%) treatment options?
What are moderate(3-10%)- severe(>10%) psoriasis?
What are severe disease treatment options?
treat with topical agents first.. If in adequate–>topical + phototherapy.. if inadequate topical+ systemic agent. Add moisturizers as needed, step down to lowest doses or potencies.
Systemic agent +/- topical agent or phototherapy. Consider BRM if comorbidities exist. If inadequate–>more potent systemic or 2 or more systemic agents in rotation +/- phototherapy–> BRM +/- others. Can also consider biologic immediately.
non biologic alone or in combination with biologics are recommended, swtiching can happen. You can start biologics immediately now as well in moderate or severe or in arthritis.
What do you avoid in congestive HF?
What about inflammatory bowel disease?
What about history of malignancy?
Avoid NSAIDS, CS, Anti-TNF.
Consider sulfasalazine, methotrexate, cyclosporine, anti-tnf, AVOID IL-17.
Avoid anti-TNF, IL-23, IL-17.
What do you avoid in liver disease?
What disease do you screen for in all systemic medications?
How do you treat psoriatic arthiritis?
Methotrexate, sulfasalazine.
Tuberculosis, HIV, Hep B & C.
In non spinal go for conventional DMARDs or TNF. NSAIDS, steroids, biologics may be considered in combined or mono. Biologics in rapid disease.
What are treatment targets for psoriasis?
What should you know about acetretin?
What causes acne?
Be a 1% or less in 3 months. Acceptable response is PASI-75 or 3%.
more rapid clearing but doesn’t work as well in monotherapy. High doses required in monotherapy. Side effects are mucosal dryness, vision impairment, and liver involvement. Should be avoided in in patients with high alcohol consumption and avoid in hepatoxicity risk drugs.
Acne is caused by distention and plugging of the pilosebaceous unit.
How do androgens effect acne?
Is a blackhead an open comedo or closed comedo?
Where does acne show up normally?
increased sebum and abnormal shedding of keratinocytes, follicles anaerobic environment leads to bacterial growth and follicular expansion and rupture exposing dermal layer leads to inflammation.
Open, Closed is whitehead.
In adolescence it’s the T zone. Inflammatory and late-stage it’s the face,chest,back,upper arms.
How can you tell acne vs folliculitis?
How can you tell acne vs hyperandrogenism?
When is the maximum duration without improvement for self treatment?
If they have folliculitis. This presents with abrupt onset,, prominent trunk distribution.
If hyperandrogenism you would see hirsutism, infrequent menses, cliteromegaly, truncal obesity.
8 weeks. If no improvement refer to a HCP.
What to know about benzoyl peroxide?
What are benzoyl peroxide’s ADR’s?
What to know about azelaic acid?
Antibacterial/antiseptic. No resistance issues, comes in 2.5-10% strength. Preferred agent for mild acne.
Irritation and allergy–> Hives swelling=d/c, lower the concentraiton, water based or wash off more tolerated than heavier products.
Similar to BP, don’t recommend it for dark skin, ADR similar to BP. Don’t recommend salacyllic acid either.
What antibiotic is preferred?
What to know about dapsone gel?
How do retinoids work?
Clindamycin 1%, Erythromycin 2% next.
Unknown activity against P.acnes. DO NOT COMBINE WITH BENZOYL PEROXIDE(makes orange brown skin discoloration).
reduce differentiation and proliferation of sebocytes, inhibit proinflammatory cytokines, increased keratinocyte shedding.
